Theory of illness causation is an important issue in all biomedical sciences, and solid etiological explanations are needed in order to develop therapeutic approaches in medicine and preventive interventions in public health. Until now, the literature about the theoretical underpinnings of illness causation research has been scarce and fragmented, and lacking a convenient summary. This interdisciplinary book provides a convenient and accessible distillation of the current status of research into this developing field, and adds a personal flavor to the discussion (...) by proposing the etiological stance as a comprehensive approach to identify modifiable causes of illness. (shrink)

Part I of this paper introduced a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

Part I of this paper introduces a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007) put forward the thesis that, at least in the health sciences, to establish the claim that C is a cause of E, one normally needs evidence of an underlying mechanism linking C and E as well as evidence that C makes a difference to E. This epistemological thesis poses a problem for most current analyses of causality which, in virtue of analysing causality in terms of just one of mechanisms or difference (...) making, cannot account for the need for the other kind of evidence. Weber (Int Stud Philos Sci 23(2):277–295, 2009) has suggested to the contrary that Giere’s probabilistic analysis of causality survives this criticism. In this paper, we look in detail at the case of medical imaging technology, which, we argue, supports the thesis of Russo and Williamson, and we respond to Weber’s suggestion, arguing that Giere’s account does not survive the criticism. (shrink)

The teratogenicity of the Zika virus was considered established in 2016, and is an interesting case because three different sets of causal criteria were used to assess teratogenicity. This paper appeals to the thesis of Russo and Williamson (2007) to devise an epistemological framework that can be used to compare and evaluate sets of causal criteria. The framework can also be used to decide when enough criteria are satisfied to establish causality. Arguably, the three sets of causal criteria considered here (...) offer only a rudimentary assessment of mechanistic studies, and some suggestions are made as to alternative ways to establish causality. (shrink)

Russo and Williamson put forward the following thesis: in order to establish a causal claim in medicine, one normally needs to establish both that the putative cause and putative effect are appropriately correlated and that there is some underlying mechanism that can account for this correlation. I argue that, although the Russo-Williamson thesis conflicts with the tenets of present-day evidence-based medicine, it offers a better causal epistemology than that provided by present-day EBM because it better explains two key aspects of (...) causal discovery. First, the thesis better explains the role of clinical studies in establishing causal claims. Second, it yields a better account of extrapolation. (shrink)

Establishing the effectiveness of medical treatments is one of the most important aspects of medical practice. Bradford Hill's viewpoints play an important role in inferring causality in medicine,...

The paper addresses the question of how different types of evidence ought to inform public health policy. By analysing case studies on obesity, the paper draws lessons about the different roles that different types of evidence play in setting up public health policies. More specifically, it is argued that evidence of difference-making supports considerations about ‘what works for whom in what circumstances’, and that evidence of mechanisms provides information about the ‘causal pathways’ to intervene upon.

According to Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007, Hist Philos Life Sci 33:389–396, 2011a, Philos Sci 1(1):47–69, 2011b ), in order to establish a causal claim of the form, ‘_C_ is a cause of _E_’, one typically needs evidence that there is an underlying mechanism between _C_ and _E_ as well as evidence that _C_ makes a difference to _E_. This thesis has been used to argue that hierarchies of evidence, as championed by evidence-based movements, tend to (...) give primacy to evidence of difference making over evidence of mechanisms and are flawed because the two sorts of evidence are required and they should be treated on a par. An alternative approach gives primacy to evidence of mechanism over evidence of difference making. In this paper, we argue that this alternative approach is equally flawed, again because both sorts of evidence need to be treated on a par. As an illustration of this parity, we explain how scientists working in the ‘EnviroGenomarkers’ project constantly make use of the two evidential components in a dynamic and intertwined way. We argue that such an interplay is needed not only for causal assessment but also for policy purposes. (shrink)

I present an alternative account of causation in the biomedical and social sciences according to which the meaning of causal claims is given by their inferential relations to other claims. Specifically, I will argue that causal claims are inferentially related to certain evidential claims as well as claims about explanation, prediction, intervention and responsibility. I explain in some detail what it means for a claim to be inferentially related to another and finally derive some implication of the proposed account for (...) the epistemology, semantics and metaphysics of causation. (shrink)

The paper considers the legal tools that have been developed in German pharmaceutical regulation as a result of the precautionary attitude inaugurated by the Contergan decision. These tools are the notion of “well-founded suspicion”, which attenuates the requirements for safety intervention by relaxing the requirement of a proved causal connection between danger and source, and the introduction of the reversal of proof burden in liability norms. The paper focuses on the first and proposes seeing the precautionary principle as an instance (...) of the requirement that one should maximise expected utility. In order to maximise expected utility certain probabilities are required and it is argued that objective Bayesianism offers the most plausible means to determine the optimal decision in cases where evidence supports diverging choices. (shrink)

Russo and Williamson claim that establishing causal claims requires mechanistic and difference-making evidence. In this article, I will argue that Russo and Williamson's formulation of their thesis is multiply ambiguous. I will make three distinctions: mechanistic evidence as type vs object of evidence; what mechanism or mechanisms we want evidence of; and how much evidence of a mechanism we require. I will feed these more precise meanings back into the Russo–Williamson thesis and argue that it is both true and false: (...) two weaker versions of the thesis are worth supporting, while the stronger versions are not. Further, my distinctions are of wider concern because they allow us to make more precise claims about what kinds of evidence are required in particular cases. (shrink)

Current research in molecular epidemiology uses biomarkers to model the different disease phases from environmental exposure, to early clinical changes, to development of disease. The hope is to get a better understanding of the causal impact of a number of pollutants and chemicals on several diseases, including cancer and allergies. In a recent paper Russo and Williamson address the question of what evidential elements enter the conceptualisation and modelling stages of this type of biomarkers research. Recent research in causality has (...) examined Ned Hall’s distinction between two concepts of causality: production and dependence. In another recent paper, Illari examined the relatively under-explored production approach to causality, arguing that at least one job of an account of causal production is to illuminate our inferential practices concerning causal linking. Illari argued that an informational account solves existing problems with traditional accounts. This paper follows up this previous work by investigating the nature of the causal links established in biomarkers research. We argue that traditional accounts of productive causality are unable to provide a sensible account of the nature of the causal link in biomarkers research, while an informational account is very promising. (shrink)

The development of causal modelling since the 1950s has been accompanied by a number of controversies, the most striking of which concerns the Markov condition. Reichenbach's conjunctive forks did satisfy the Markov condition, while Salmon's interactive forks did not. Subsequently some experts in the field have argued that adequate causal models should always satisfy the Markov condition, while others have claimed that non-Markovian causal models are needed in some cases. This paper argues for the second position by considering the multi-causal (...) forks, which are widespread in contemporary medicine (Section 2). A non-Markovian causal model for such forks is introduced and shown to be mathematically tractable (Sections 6, 7, and 8). The paper also gives a general discussion of the controversy about the Markov condition (Section 1), and of the related controversy about probabilistic causality (Sections 3, 4, and 5). (shrink)

Thinking about illness causation has a long and rich history in medicine. After a hiatus in the 1990s, the last one-and-a-half decades have seen a surge of publications on causality in the biomedical sciences. Interestingly, this surge is visible not only in the medical, epidemiological, bioinformatics, and public health literatures, but also among philosophical publications. In this essay, I review and discuss one most recent addition to the literature, "Causality: Philosophical Theory Meets Scientific Practice" written by philosophers Phyllis Illari and (...) Federica Russo about causality in the sciences, and particularly about the health sciences. (shrink)

This article examines two theses formulated by Russo and Williamson in their study of causal inference in the health sciences. The two theses are assessed against evidence from a specific case in the social sciences, i.e., research on the institutional determinants of the aggregate unemployment rate. The first Russo–Williamson Thesis is that a causal claim can only be established when it is jointly supported by difference-making and mechanistic evidence. This thesis is shown not to hold. While researchers in my case (...) study draw extensively on both types of evidence, one causal claim out of the three analyzed is established even though it is exclusively supported by mechanistic evidence. The second Russo–Williamson Thesis is that standard accounts of causality fail to handle the dualist epistemology highlighted in the first Thesis. I argue that a counterfactual-manipulationist account of causality—which is endorsed by many philosophers as well as many social scientists—can perfectly make sense of the typical strategy in my case study to draw on both difference-making and mechanistic evidence; it is just an instance of the common strategy of increasing evidential variety. (shrink)

Evidence-based medicine (EBM) makes use of explicit procedures for grading evidence for causal claims. Normally, these procedures categorise evidence of correlation produced by statistical trials as better evidence for a causal claim than evidence of mechanisms produced by other methods. We argue, in contrast, that evidence of mechanisms needs to be viewed as complementary to, rather than inferior to, evidence of correlation. In this paper we first set out the case for treating evidence of mechanisms alongside evidence of correlation in (...) explicit protocols for evaluating evidence. Next we provide case studies which exemplify the ways in which evidence of mechanisms complements evidence of correlation in practice. Finally, we put forward some general considerations as to how the two sorts of evidence can be more closely integrated by EBM. (shrink)

This contribution claims that the two fundamental notions of causation at work in the health sciences are manipulative and mechanistic, and investigates what kinds of evidence matter for the assessment of causal relations. This article is a development of our 2007 article, ‘Plurality of Causality’, where we argue for a pluralistic account of causation with an eye to econometrics and a single medical example. The present contribution has a wider focus, and considers the notion of evidence within a whole range (...) of disciplines belonging to the health sciences. Section 1 addresses the relations between kinds of evidence and causal accounts, and it is shown how different notions of causation can be employed in various medical cases. Section 2 calls attention to issues crucial for any adequate epistemological theory of causation, such as the distinctions between types and tokens, observational and experimental regimes, explanation and prediction. Lastly, the notion of context is articulated, highlighted in its role in the assessment of causal links. All these issues are tackled in the framework of what we label a ‘bottom–up’ epistemology. (shrink)

Not only has the philosophical debate on causation been gaining ground in the last few decades, but it has also increasingly addressed the sciences. The biomedical sciences are among the most prominent fields that have been considered, with a number of works tackling the understanding of the notion of cause, the assessment of genuinely causal relations and the use of causal knowledge in applied contexts. Far from denying the merits of the debate on causation and the major theories it comprises, (...) this paper is meant as a stimulus for theorists of causation in the philosophy of biomedicine, with a focus on clinical matters. Without aiming at putting forward an original theory of causation and starting from the narration of two actual but paradigmatic cases at the joints between biomedical research and clinical practice, we want to point out that some pathological situations addressed by molecular medicine actually prove resistant to some of our major epistemological accounts of causal explanation. Given this scenario, which is very frequent in our hospitals, our analysis aims to provide a stimulus for the debate among theorists of causation in biomedicine interested in real cases in science in practice. We believe that this might in turn encourage some more general rethinking of the complex intertwinement of science, philosophy of science and ethics, as well as of the role of philosophy of science for clinical medicine itself. (shrink)

Despite the consensus promoted by the evidence-based medicine framework, many authors continue to express doubts about the superiority of randomized controlled trials. This paper evaluates four objections targeting the legitimacy, feasibility, and extrapolation problems linked to the experimental practice of random allocation. I argue that random allocation is a methodologically sound and feasible practice contributing to the internal validity of controlled experiments dealing with heterogeneous populations. I emphasize, however, that random allocation is solely designed to ensure the validity of causal (...) inferences at the level of groups. By itself, random allocation cannot enhance test precision, doesn’t contribute to external validity, and limits the applicability of causal claims to individuals. (shrink)

In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. Despite these, I argue (...) that the RWT is historically workable, given a small number of modifications. I then expand Russo and Williamson’s account. I first develop their suggestion that causal relationships in medicine require some kind of evidence of mechanism. I begin with a number of accounts of mechanisms and produce a range of consensus features of them. I then develop this consensus position by reference to the two historical case studies with an eye to their operational competence. In particular, I suggest that it is mechanistic models and their representations which we are concerned with in medicine, rather than the mechanism as it exists in the world. -/- I then employ these mechanistic models to give an account of the sorts of evidence used in formulating and evaluating causal claims. Again, I use the two human viral oncogenesis cases to give this account. I characterise and distinguish evidence of mechanism from evidence of difference-making, and relate this to mechanistic models. I then suggest the relationship between types of evidence presents us with a means of tackling the reference-class problem. This sets the scene for the final chapter. Here, I suggest the manner in which these two different classes of evidence become integrated is also reflected in the way that developing research programmes change as their associated causal claims develop. (shrink)